Month: November 2012

Toys for Girls and Boys

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I don’t know why it comes as a surprise every year; but as soon as the pumpkins are sold out and the fireworks over, supermarkets start playing Noddy Holder and for the next month and a half we are reminded constantly of the upcoming festive season. The desperate panic felt as I realise how many presents I need to buy is dampened only by copious amounts of mulled wine. There is, however, one person for whom I actually look forward to buying a Christmas present; my godson Sam. Sam is four years old and extremely passionate about trains, fire engines, tractors…in fact, give him any sort of miniaturised mode of transport and he’ll be happy for hours. This love of miniature machines is typical for a boy of his age whilst many of his female contemporaries will be putting altogether different toys on their Christmas list: dolls, tea sets, play kitchens to name but a few. Indeed, once again this year the majority of young boys and girls will have their stockings filled with gender-appropriate toys, but what causes these preferences?

Last year, Dr. Laura Nelson (a neuroscientist) persuaded London’s largest toy shop ‘Hamleys’ to stop marketing their toys as being either ‘for girls’ or ‘for boys’. She felt that such marketing influenced the types of toys children chose, therefore reinforcing gender stereotypes: girls playing with tea sets encourages domestic, passive playtime, whereas boys might engage in more active and aggressive play if given a pirate ship. While we already assume that environmental factors (toys, parents, friends) can influence a child’s gender-identity, are there any biological reasons why girls like ‘sugar and spice and everything nice’, while boys are happier playing with a lorry that turns into a robot?

Since it would be very hard, not to mention unethical, to hide a child away from all gender-biasing environmental influences, the majority of current research is based on animal studies; specifically monkeys! Since most monkeys have no interest to advertising campaigns and few have played with a teddy or toy car before, they make pretty good ‘naive’ experimental subjects. Prof. Melissa Hines and her fellow scientists from Cambridge allowed male and female vervet monkeys to ‘take their pick’ of masculine and feminine children’s toys, then recorded how long they spent playing with each one. As it turns out, female vervet monkeys spent more time with the typical girls’ toys, while male monkeys spent more time with typical boys’ toys. This sex-determined preference for different types of toy suggests that there could actually be fundamental differences between male and female brains; perhaps not just in monkeys, but in humans too.

So does gender change the wiring of a child’s brain, biasing their choice towards more gender-appropriate toys? Professor Gerianne Alexander studied three month-old babies – or rather, how these babies looked at toys. The longer a baby looks at something, the more he or she is believed to like that object. The length of babies’ glances at either dolls (feminine), trucks (masculine) or balls (neutral) were measured and then compared to the level of testosterone they were exposed to in the womb. Testosterone is made by both boys and girls but boys produce much more since they have… well, testes. Interestingly, Gerianne found that the level of testosterone in the womb correlated with how much the babies liked typically masculine toys. So the lads swimming around in more testosterone looked longer at the trucks, while girls who weren’t exposed to high levels of testosterone looked longer at the dolls.

Incredibly enough, in a similar experiment with newborn babies (conducted just 24 hours after birth) Prof. Simon Baron-Cohen and his colleagues found that, even at this early time-point, (at least the earliest possible considering hospital guidelines), there seems to be biological differences between the sexes. These studies suggest that the level of circulating testosterone in the womb may be enough to impact brain development and possibly behaviour, even before Christmas TV adverts can brainwash them.

Further proof of the gender-biasing effect of prenatal testosterone comes from cases of congenital adrenal hyperplasia (CAH). CAH is a genetic disorder which leads to the overproduction of testosterone. CAH is usually diagnosed at birth and can be successfully treated with steroids. Children suffering from this disorder usually go on to lead a totally normal life, despite their brain’s prenatal exposure to high levels of testosterone. Interestingly, though, Prof. Hines has found that girls with CAH tend to be tomboys through their childhood. They are seen to play more like boys, favouring ‘rough and tumble’ games and typical boys’ toys over more feminine play times. So, levels of prenatal testosterone seem to predict toy choice more accurately than the actual sex of the child.

I should emphasise that while prenatal testosterone levels might correlate well with the tricky choice of Action Man vs. Barbie, it doesn’t necessarily mean that testosterone causes kids to pick one or the other. Impatient parents can’t just inject their kids with testosterone to make Christmas shopping easier. It’s also likely that the timing of exposures to certain hormones may influence the brain in different ways. What’s interesting, though is that something as ubiquitous as toys can be used as a way of investigating the science behind gender-stereotyped behaviours. Also, something tells me my godson would have plenty of excuses to be ungrateful if I get him a My Little Pony this year. Best start looking for a space rocket…

Post by: Natasha Bray

The Junk in Your Genetic Trunk

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Almost every cell in our body contains, at its centre, a small tangle of DNA. The genetic information this DNA holds is vital for every aspect of a cell’s life. As a result, it can have a direct impact on our own health. Developing an understanding of how this genetic information works is an important goal of medical science.

One of the most significant breakthroughs in our understanding came around 10 years ago when scientists successfully sequenced the human genome. This research provided a massive leap in terms of our understanding of genetics. However, it also brought with it a number of unexpected surprises. The most baffling discovery from the human genome project was how few genes we humans actually have.

A gene is a portion of DNA that contains usable information, in the form of a relatively short genetic code. This information tells your cells how to make important cellular components – proteins. We normally think of protein in terms of food but it turns out we literally are what we eat. The dry mass of our cells is made mostly from fat and protein, with a dash of carbohydrates. These proteins are hugely important to our cells. They act like tiny machines, rushing around the cell carrying out various intricate and essential jobs.

Interestingly only a small amount (around 2%) of our total DNA actually codes for usable proteins. The rest of the DNA doesn’t contain any instructions on how to make protein and is therefore sometimes called ‘junk DNA’.

It turns out human beings have only around 25,000 functioning genes. This may sound like a lot but when you consider that a round worm has 19,000 this number suddenly seems much less impressive. This was a big surprise since when the human genome project began it was assumed that, due to the complexity of human beings we would have a lot of genes, certainly many more than a lowly worm. No offence to round worms but we are way more complex. I mean they only have 970 cells, compared to our 60 trillion. It’s not a competition but if it were, we’d be winning.

So how come we only have 30% more protein-coding genes than a simple roundworm and why is so much of our DNA junk?

It turns out that we were a little too quick to judge these non-coding regions as ‘junk’. In fact we now recognise that this supposedly ‘junk’ DNA actually performs some very important jobs.

Back in September the ENCODE project published 30 papers showing how ‘junk’ DNA can actually influence the way our genes are read. The non-coding or ‘junk’ regions can help switch genes on or off which, in turn, influences whether a cell makes a certain protein or not. Non-coding DNA can recruit machinery in the cell which can either promote or hinder the process of turning a gene into a protein. The non-coding DNA can also be actively modified by a process called methylation, which switches off genes. Methylation can occur at any point in your life and may represent a way by which our environment and lifestyle can actually change our DNA. This is one of many ways our underlying genetic code can be modulated and is called an ‘epigenetic’ alteration. Such epigenetic changes might go some way to explaining why genetically identical twins, who have lived quite separate lives, often become less alike as they age.

[youtube http://www.youtube.com/watch?v=AV8FM_d1Leo]

Another way non-coding DNA switches genes on and off is by controlling how DNA is stored. If you were to unwind the DNA from all the cells in your body and stand it end to end it would reach to the sun and back….6 times. The reason the DNA can fit into our tiny cells is because it is wound up tightly on miniscule round structures called histones. It’s a bit like winding yarn round a spool – it takes up less space. When DNA is tightly wound around histones the cell machinery that ‘reads’ the genetic message can’t access the genes. Non-coding DNA can recruit proteins which unwind the DNA, exposing certain genes and allowing the cell to make its corresponding protein. It’s essentially genetic peek-a-boo.

Another layer of complexity is provided by the fact that once a gene is switched on, the instructions concerning how that gene is interpreted can be changed. This means that the same gene can make several slightly different proteins.

The ability to control how, where and when to switch on a gene provides our cells with an amazing ability to adapt, specialise and respond to their environment. Although fundamentally important, knowing what genes are is only half the story in human genetics. Projects like ENCODE are helping shed light on the nuanced intricacies of how our genes are regulated and what makes human beings so complicated – or at least more complicated than round worms. Ultimately the understanding we’re beginning to develop will not only help tackle diseases, but will also help us understand what makes us who we are.

Post by: Liz Granger

Twitter: @Bio_Fluff

Could Jennifer Aniston hold the key to memory formation?

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Ever since her leap to fame as Rachel on the popular TV sitcom Friends, Jennifer Aniston has been one of the most recognisable actresses in the world. Now, scientists believe that the discovery of brain cells responding specifically to pictures of Jennifer Aniston  may hold the key to understanding how the brain forms memories.

Imagine walking down a busy street and noticing a friend walking on the other side of the road. Even following just a brief glance from any angle your brain allows you to recognise your friend and conjure up a whole host of memories about that person; including their name, their personality and perhaps something really important you were meaning to talk to them about. This scenario provides a perfect example of how efficient the brain is when it comes to memory storage and retrieval. However, scientists still have a very limited understanding of how all this can occur so quickly and faultlessly.

The idea that single brain cells can respond exclusively to specific objects/people is not a new one. However this idea is not widely accepted in the scientific community. One notable sceptic was Jerry Lettvin, a researcher from Massachusetts Institute of Technology, who argued against the simplification of memory function in the late ‘60s.

Lettvin expressed his criticism of this idea through an example. He described a hypothetical brain cell specialised to respond only to the sight of your grandmother (a ‘grandmother cell’). This cell could then be linked with and activate many other cells responsible for memories of your grandmother such as the smell of her cooking or the sound of her knitting. Through this example Lettvin highlighted a number of problems with such a simple set-up; if the brain did possess a cell to recognise every single object you’ve encountered then surely the brain would run out of space at some point? Moreover, what would happen if you lost one of these cells? Would you be unable to recognise your grandmother any more?

Image credit: Jolyon Troscianko

Despite its ridicule, the ‘grandmother cell’ theory has recently been revived by the discovery of single cells in the human brain which respond specifically to recognisable people. These cells were discovered by a team operating in Los Angeles, California led by Rodrigo Quian Quiroga from the University of Leicester who had the unique opportunity of recording from single cells in the brains of awake, behaving humans.

The ability to record single cell activity in awake human patients is clearly very rare. However, the LA team were able to conduct their study using a special group of patients undergoing treatment for severe epilepsy. When a patient with severe epilepsy does not respond to medication, the faulty brain region responsible for seizure generation must be be removed. As this area usually differs between patients, a surgeon will implant an electrode (see left) into the brain which will record electrical activity in various locations and tell the surgeon which area needs to be removed. This allowed Quiroga and his team to record single-cell activity from awake, behaving humans.

They showed these patients many pictures of objects and people in an attempt to discover what these brain cells responded to. In one of their first experiments they found a cell that appeared to respond specifically to pictures of Jennifer Aniston which they later named the ‘Jennifer Aniston cell’.

To ensure that this cell was actually responding to Jennifer Aniston and not some other feature of the pictures they were using (for example, her blonde hair or maybe the contrast of her compared to the background etc) they tested the cell using a huge range of Jennifer Aniston pictures. These included pictures of her face from various angles, her whole body and some of her standing next to (her then husband) Brad Pitt. These pictures were shown to the patient multiple times and mixed in with pictures of other celebrities and family members.

The results were remarkable. The cell did not respond to any other person (around 80 other people were shown) but responded specifically to pictures of Jennifer Aniston. Interestingly the cell did not care whether it was a head shot or a picture of her whole body – two views which, from an image processing perspective, are very different. However, the cell did not like Brad Pitt! Any time a shot of Jennifer Aniston and Brad Pitt together was shown the cell refused to respond. This baffled the researchers. Why would the cell fire specifically to Jennifer Aniston but only when she was on her own?

The answer came when they found that this cell also responded (not as much as to Jennifer Aniston but enough to be significant) to Lisa Kudrow, the actress who plays Phoebe on Friends. Quiroga hypothesised that the cell was not actually responding to a specific person, but instead responding to the ‘concept’ of ‘Rachel from Friends‘. When Jennifer Aniston was shown on her own, the patient was reminded of Rachel and the cell would fire. When Jennifer Aniston was shown next to Brad Pitt, that was Jennifer Aniston the actress and not Rachel, and the cell did not respond. Thus the cell, once thought to be a ‘Jennifer Aniston cell’, became known instead as a ‘concept cell’. These ‘concept cells’ would form a key part of a hypothesis Quiroga was building regarding memory formation.

Recording from new patients, Quiroga and his team found multiple examples of these ‘concept cells’. For example, cells were found which responded to Halle Berry on her own and Halle Berry in costume as ‘Catwoman’ (pictures where her face is almost entirely obscured by the costume). A cell was also seen responding exclusively to either Luke Skywalker or Yoda; a Star Wars concept cell?

To further cement the ‘concept cell’ theory, Quiroga’s team investigated whether these cells would also respond to non-visual methods of triggering these concepts. To do this they used the ‘text to speech’ function on their laptop playing a robotic voice speaking the celebrity’s name. Amazingly, this had the same effect – that is, the cell that responded to pictures of Halle Berry, also responded to the spoken words ‘HALLE BERRY’. The pathways for the processing of visual and auditory information are largely separate and have limited cross-over but somehow, these two types of information are being relayed to one individual cell.

This raises some interesting questions concerning what happens when we form new memories. Imagine for example that you meet a new person and do not catch their name. Your brain will store a visual image of this person, linking it to a ‘concept cell’. Days or weeks later you may then learn the person’s name. Does this mean that this auditory information will create new links, through a completely different pathway, right back to the original ‘concept cell’ for this person?

If correct, this type of specificity in linking parts of the brain together is truly remarkable. Quiroga believes the ‘concept cells’ he has unearthed in these studies represent the building blocks of our memories and are crucial for forming associations necessary for storing and retrieving multifaceted memories. Quite a claim, but he is uneasy about labelling them ‘grandmother cells’ as this simplifies what many believe to be a complex process. The next stage of this research will be crucial as Quiroga aims to investigate how these ‘concept cells’ communicate with each other and how the timing of each cell’s activity may be the key to linking them – and therefore, your memories – together.

All work described here is summarised in the following review by Rodrigo Quian Quiroga (subscription needed):

Post by Oliver Freeman @ojfreeman

Sleep deprivation on the campaign trail

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The gruelling final few months of the presidential election campaign are notorious in political circles. Candidates get by on as little as four hours sleep most days due to huge demands on their attention and judgement as the campaign reaches its zenith. With the current election teetering on a knife edge, presidential candidates Barack Obama and Mitt Romney will have to pack as much into their schedules as possible whilst they power toward the finish line.

But what kind of effect does chronic sleep deprivation have and what sort of mental challenges must the candidates endure?

Ever since the introduction of artificial lighting two centuries ago, the time the average person spends sleeping has begun to decrease. Whilst the precise role of sleep on our physiology and function is not yet clear, the effects of its absence are well-documented:

It has been shown that even mild sleep deprivation can ‘fog’ the mind. One study, carried out by an Australian research group, found that mild sleep deprivation caused similar deficits to those seen following alcohol consumption. Specifically, performance on a computer-based movement task was impaired equally by both 22 hours without sleep and having a blood-alcohol content of 0.08% (above the legal driving limit).

Both movement-related tasks, such as this, and non-movement-related tasks are well-documented to be affected by sleep deprivation. In fact, most executive functioning tasks are inhibited! MRI scans have shown that activity in an area of the brain known as the prefrontal cortex declines when subjects are sleep-deprived. This part of the brain integrates all sorts of processes including perception, movement and verbal reasoning. As a result, any task that requires a lot of attention becomes difficult or, in some cases, almost impossible. Any form of novelty, including being placed in an unusual situation or answering unexpected questions becomes difficult.

Obama’s campaign trail Oct 24-25. Obama travelled over 6,000 miles in just two days. His schedule included several TV interviews and rallies. Similarly, in October alone Mitt Romney engaged in 61 campaign events across America.

Sleep deprivation is also known to negatively affect a person’s ability to memorise new information, a problem which can have a serious knock-on effect on their ability to plan and make decisions. The part of the brain which deals with memory is known as the hippocampus. Scientists believe that, when learning something new, sleep allows connections in this brain region to be modified and strengthened which consolidates memories into more permanent forms. Thus it’s not surprising that not getting enough sleep can lead to memory problems. Indeed, even when awake, neurons in this part of the brain in sleep-deprived individuals don’t fire as frequently or function as they should.

Another major problem anyone who has experienced sleep deprivation will recognise is the affect it can have on our emotions. Of course, it is common for people to become short-tempered and irritable when tired. However, research has shown that lack of sleep can also lead to more serious emotional changes including a reduction in an individual’s ability to solve problems using moral reasoning. Rather than making decisions based upon internal moral values, sleep-deprived people can shift to more external, rule-based decision making (more akin to the ‘black and white’ reasoning used by many children). Emotional memory also seems to be impaired, making it more difficult for a person to empathise with others.

People also become hungrier when they aren’t sleeping. This is not thought to be caused by extra energy expenditure (basal metabolic rate when asleep is 90% of that when awake) but instead, is believed to be due to an adverse increase in ghrelin (a hormone that causes hunger) and concurrent decrease in leptin (a hormone which prevents hunger).

All of these impairments combine to induce a haze that puts incredible stress on the individual. That two older men (Obama and Romney are 51 and 65 respectively) can debate, write speeches, plan meetings, strategise and campaign whilst mentally and physically strained is testament to their indefatigability. However, with recent polls showing less than 1% between the two rivals, even the smallest misjudgement or gaff could mean the difference between despair or delight.

Given the campaign suspension from both candidates during hurricane Sandy, it’s possible that each enjoyed a precious full night’s sleep during this critical period. Now that the race has returned to its usual punishing final sprint, it may be that whoever can best deal with the sleepless nights will be at a crucial and possibly decisive advantage.

Post by: Chris Logie